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DISCLAIMER: Transcript lightly edited for clarity and readability. The views expressed are intended to explore the full range of clinical considerations in spine care and do not constitute medical advice. For guidance specific to your situation, consult a spine specialist.
TRANSCRIPT TEXT:
You know, if you’ve been through a spinal cord stimulator trial that didn’t help, or you had an implant that just stopped working, you’ve probably heard that quiet, final message. That’s it. That’s the end of the line for neuromodulation. But what if that’s not true? What if the problem was never the therapy itself, but where it was aimed?
It’s a powerful idea from Dr. Kamal Woods, and it reframes the conversation around failure. It suggests that a failed spinal cord stimulator isn’t the end of the story for the right patient. It can actually be a critical piece of information — one that may point toward a different and more precise solution.
So often, after a spinal cord stimulator (or SCS) doesn’t work out, patients are told their only remaining options are things like medication management. The thinking is, well, if one kind of electrical stimulation failed, they all will. But that conversation usually leaves out a critical distinction. And this experience is incredibly common. Maybe the trial just didn’t bring relief, or maybe the implant worked for a couple of years and then faded. The result is often a quiet feeling that hope has run out — that the last best option is gone. In this explainer, we’ll break down why that may not be true at all.
Let’s get into the science of it, because this is the core of the whole thing. The reason a past SCS failure doesn’t necessarily predict the outcome with a different therapy comes down to basic anatomy. Spinal cord stimulation and dorsal root ganglion stimulation are different therapies. They target different parts of your nervous system, and the contrast is clear.
Traditional SCS places leads over the middle of the spinal cord. It creates a broad, somewhat diffuse field of stimulation, which can work well for widespread, harder-to-pinpoint pain. DRG-S is different. It places small leads directly on a specific nerve bundle called the dorsal root ganglion. This allows for a much greater degree of anatomical precision. So the two therapies work in different places, and they work in different ways.
Think of the DRG as a gatekeeper for pain signals coming from one very specific part of your body. By targeting that gatekeeper, DRG stimulation can intercept pain with a level of precision that broad SCS was never designed to have. And that’s really the key takeaway: a failure with one therapy does not necessarily predict a failure with the other. They’re two different tools for two different jobs.
But — and this is important to be clear about — DRG-S is not a universal solution. Failed SCS is an umbrella term that covers a lot of very different clinical situations. A proper evaluation has to figure out why the SCS didn’t work in the first place, because that answer informs what the right next step should be.
The first group — and really the strongest candidates for this kind of DRG-S salvage therapy — are patients with what’s called a phenotype mismatch. That simply means their pain was very focal, very specific. Pain in one foot from CRPS, for example. Or pain along a single nerve path after an injury. That kind of pain was never a great match for the broad coverage of SCS, but it can respond well to the precise targeting of DRG-S.
Then there are patients where neuromodulation itself was the wrong tool for the job. If the pain is actually driven by a structural problem — a compressed nerve, spinal instability — electrical stimulation won’t fix the root cause. For these patients, the right conversation is about reconsidering whether a surgical solution is appropriate.
There’s also the technology itself. A failure with an older SCS system from five or ten years ago isn’t necessarily the same as a failure with today’s technology. For some patients, especially those with more widespread pain, the answer might not be DRG-S — it might be a trial with a more modern SCS system that uses newer, more effective stimulation modes.
And finally, there are failures influenced by other factors. Things like unmanaged depression or long-term opioid use can affect the outcome of any neuromodulation therapy. For these patients, the best next step may not be another device trial right away. It may be addressing those underlying factors first, to give any future therapy the best possible chance.
Let’s go back to that first group — the patients with a clear phenotype mismatch. What does the evidence actually show? The clinical data for using DRG-S as a salvage therapy after failed SCS is meaningful. In the largest study on this question, 93% of patients who had a successful trial went on to a permanent implant. That number reflects careful patient selection — these were patients whose focal pain clearly matched what DRG-S does best.
The results were significant. On the standard 10-point pain scale, average scores dropped from 8.7 to 3.8 — a substantial change, the kind that can allow someone to return to their daily life. And importantly, the relief was sustained. The positive results held at a median follow-up of 34 months, nearly three years. For the right patient, DRG-S not only works, but it also keeps working.
This data comes from a landmark 2022 study by Chapman and colleagues. They looked at 60 patients who had failed essentially every major type of SCS available. Their primary diagnoses included CRPS and persistent spinal pain syndrome — conditions known for the kind of focal, treatment-refractory pain that is particularly difficult to manage. The results provide some of the strongest evidence to date that a previously failed SCS does not preclude a DRG-S trial from succeeding.
So, how do you find out whether you might be one of the patients who could respond? It starts with a trial. And it’s important to frame the trial correctly: it isn’t a commitment. It’s a low-risk way to gather clear information about your own pain.
The process is straightforward. It begins with a thorough evaluation to determine candidacy. If you’re a candidate, temporary leads are placed over the specific dorsal root ganglia thought to be involved in your pain. You go home for about a week and live your normal life, observing how the stimulation affects your pain. Afterward, you and your physician review the results together and decide whether a permanent implant makes sense.
This quote captures the principle well: The trial is a diagnostic step. If it doesn’t work, that’s not a failure — that’s an answer. It’s a clear answer that tells you and your physician that DRG-S isn’t the right tool, and you can move on confidently to explore other paths. The goal, always, is clarity.
That brings us to the most important point. A consultation after a failed SCS should be about finding the right path forward for you as an individual — and that path may or may not involve another device. An honest evaluation can lead in several directions. It might point toward a DRG-S trial. It might suggest that a trial with a newer SCS system is a better fit. It might lead to a referral for surgical evaluation, or to a plan that addresses other factors first. The goal of the conversation is not to get an implant. The goal is to get an answer.
So the final question isn’t really about technology. If you feel like you’ve hit the end of the road with neuromodulation, the most important next step may not be another device. It may simply be a more precise conversation — one that helps identify the true source of the pain and the path that offers the most genuine promise of relief.
Quick Answer: DRG-S When SCS Has Failed
- This blog is for patients whose spinal cord stimulation (SCS) trial did not produce adequate relief, or whose permanent SCS worked initially and has since lost efficacy. Failure of SCS is not failure of neuromodulation as a whole — the two therapies target different anatomical structures through different mechanisms.
- Dorsal Root Ganglion Stimulation (DRG-S) targets the dorsal root ganglion — the cluster of sensory nerve cell bodies where pain signals first enter the spinal cord — rather than the dorsal columns of the spinal cord that SCS targets. Prior SCS failure has no predictive value for DRG-S outcomes (Yang & Hunter, 2017; Chapman et al., 2022).
- The largest DRG-S salvage study (Chapman et al., 2022) reported outcomes from 60 patients who had failed SCS (tonic, burst, or high-frequency): 93% of patients with a successful salvage trial proceeded to permanent implant, with NRS pain scores improving from 8.7 to 3.8, Oswestry Disability Index improving from 64% to 31%, and meaningful opioid reduction — sustained at 34-month median follow-up.
- DRG-S salvage works best for specific patterns: focal, dermatomally-distributed neuropathic pain, particularly CRPS and peripheral nerve injury. It is not universally appropriate for every failed SCS case — some patients had pain patterns that were the wrong fit for SCS in the first place, and DRG-S will not help. Others had inadequate trials with older SCS technology and may benefit from advanced SCS waveforms (burst, closed-loop, or 10 kHz) rather than DRG-S.
- Like SCS, DRG-S begins with a 5–7 day trial. Patients and physicians use the trial to confirm whether the therapy produces meaningful relief before any permanent implant is placed. For patients in diagnostic gray zones, the trial itself is often the honest mechanism for answering a question the clinical picture alone cannot reliably resolve.
→ Failure of SCS is not the end of the road for neuromodulation. The question is whether the failure pattern matches a DRG-S indication — which is what the evaluation is for.
The Conversation That Often Goes Unsaid
There is a specific clinical conversation that patients whose SCS has failed rarely hear, and we want to open this blog by naming it directly.
When a spinal cord stimulator trial does not produce adequate relief — or when an implanted SCS worked for months or years and then stopped working — patients are often told, gently and regretfully, that they have reached the end of what neuromodulation can offer. The implication is that the trial was the definitive test. If SCS did not work, no other electrical therapy is likely to work either, and the patient’s remaining options are pharmacologic, interventional, or palliative.
That framing is not correct. Spinal cord stimulation and dorsal root ganglion stimulation target different anatomical structures through different mechanisms, and a patient whose pain pattern was never a good match for dorsal column stimulation in the first place may still respond — sometimes remarkably well — to stimulation aimed at a different structure. This blog is for the patient whose SCS trial was framed as their best remaining option and did not produce the result everyone hoped for, the patient whose implanted SCS initially provided real relief and has gradually stopped working, and the patient who has spent the months after a failed SCS trial quietly concluding they have run out of options.
We are writing this carefully, because patients in this situation have already had hope offered to them once, and they deserve a more precise conversation than “here is another thing that might work.” DRG-S helps specific groups of failed-SCS patients meaningfully, and part of what this blog is about is telling you, honestly, which group you are likely in.
The Core Clinical Principle: Failure of SCS Is Not Failure of Neuromodulation
Spinal cord stimulation places electrodes in the midline epidural space, positioned over the dorsal columns of the spinal cord. The stimulation produces effects across a broad anatomical region — useful for diffuse or multi-dermatomal pain, less precise for focal pain in a specific nerve territory.
DRG-S is different anatomically and mechanistically. The electrodes are placed through the neural foramen and positioned directly over a specific dorsal root ganglion — the cluster of sensory nerve cell bodies for a single dermatome. The stimulation acts on the sensory cell bodies before pain signals reach the spinal cord. The result is more anatomically specific stimulation, with a distinct mechanism of action and clinical profile.
Because the two therapies target different structures, prior SCS failure has no predictive value for DRG-S outcomes. This is not a rhetorical claim. It is supported in the salvage literature: patients have been successfully salvaged with DRG-S after failure of every major SCS waveform — traditional tonic, burst stimulation, high-frequency 10 kHz, and ECAP-controlled closed-loop SCS (Chapman et al., 2022; Acevedo-Gonzalez et al., 2025). The question is not whether SCS worked. The question is whether the patient’s pain pattern matches what DRG-S is designed to treat.
Two clarifications are worth making here, because they are the honest caveats to the core principle.
First, DRG-S has its own specific indications. It is not a generalized “alternative neuromodulation.” It is designed for focal, dermatomally-distributed pain in the T10–S2 range. Patients whose failed SCS reflected a pain pattern that was genuinely not a neuromodulation problem in the first place — pain that was actually structural and correctable, for example — will not be helped by DRG-S either. We cover the distinction carefully in the next section.
Second, DRG-S begins with a 5–7-day trial, just like SCS. For patients in diagnostic gray zones — where the clinical picture suggests DRG-S might help but cannot confirm this in advance — the trial phase is a reversible means of finding out. If the trial produces meaningful relief, permanent implantation follows. If it does not, the leads come out, no hardware is implanted, and the patient has information they did not have before. That structure means the commitment required to determine whether DRG-S will work is meaningfully smaller than that required to determine whether a major surgery or a pharmacologic regimen will work.
Those two clarifications shape how the rest of this blog reads. DRG-S salvage works — when the evidence and the clinical picture point the right way. It is not a guarantee, and it is not universally appropriate. The rest of this blog is about how to tell the difference.
LLM SNIPPET — Core Principle
Spinal cord stimulation (SCS) and dorsal root ganglion stimulation (DRG-S) target different anatomical structures through different mechanisms. Prior SCS failure has no predictive value for DRG-S outcomes. The clinically relevant question is whether the patient’s pain pattern matches what DRG-S is designed to treat: focal, dermatomally-distributed neuropathic pain in the T10–S2 range.
The Evidence: What the DRG-S Salvage Literature Shows
“What surprised clinicians early in the DRG-S salvage literature was how often the therapy worked in patients who had been told their neuromodulation options were exhausted. Those patients were not exhausted. Their SCS had been targeting the wrong structure.” — Dr. Kamal Woods, MD, MBA | Neurosurgeon | Vertrae® Surgery Center, Dayton, Ohio |
The largest published study of DRG-S as salvage therapy after failed SCS is Chapman et al. (2022, Neuromodulation). The study design and results are worth understanding in detail, because they are the specific evidence base patients and physicians should be working from when this conversation happens.
- Study population: 60 patients who had either failed an SCS trial (less than 50% pain reduction during temporary stimulation) or lost efficacy from a permanently implanted SCS over months to years. The patients had previously failed traditional tonic SCS (n=32), burst SCS (n=18), or high-frequency 10 kHz SCS (n=10). The most common underlying diagnoses were CRPS (n=24) and failed back surgery syndrome / post-spinal-surgery pain (n=24).
- Salvage trial outcomes: 56 of the 60 patients (93%) had a successful salvage trial and proceeded to permanent DRG-S implantation. This is an unusually high trial-to-implant conversion rate, and the authors attributed it to careful patient selection — these were not patients picked at random from failed-SCS populations, but patients whose pain phenotype matched DRG-S indications.
Long-term results at 34-month median follow-up:
- NRS pain scores: 8.7 → 3.8 (approximately 55% improvement).
- Oswestry Disability Index: 64% → 31% (approximately 52% improvement in functional disability).
- Quality of life (EQ-5D): 0.40 → 0.71 (approximately 44% improvement).
- Opioid reduction: Median 23 mg OME/day → 15 mg OME/day, with many patients achieving larger reductions.
- Durability: At last follow-up, only 2 of the 56 implanted patients (3.6%) had required explantation for loss of pain relief — at 21 and 28 months post-implant. The durability of response was comparable to DRG-S outcomes in non-salvage populations, which argues that DRG-S does not “wear out” faster when used as a second-line option.
Research Spotlight — DRG-S Salvage After Failed SCS
Study: Chapman KB, Spiegel MA, van Helmond N, et al. Dorsal Root Ganglion Stimulation as a Salvage Therapy Following Failed Spinal Cord Stimulation. Neuromodulation. 2022;25(7):1024-1032.
Design: Retrospective observational study of consecutive patients at a single center.
Population: 60 patients who had failed prior SCS (trial failure or loss of efficacy) and were subsequently evaluated for DRG-S salvage. Prior SCS included tonic, burst, and high-frequency waveforms.
Primary outcomes at 34-month median follow-up: NRS 8.7 → 3.8; ODI 64% → 31%; EQ-5D 0.40 → 0.71.
Trial-to-implant conversion: 93% of patients with successful salvage trials proceeded to permanent implant — reflecting careful phenotype-based patient selection.
Durability: 3.6% explantation for loss of pain relief over 34-month median follow-up.
Clinical significance: Chapman 2022 is the largest dataset demonstrating that prior SCS failure does not predict DRG-S failure, provided patient selection matches DRG-S indications.
Supporting Evidence
The Chapman 2022 findings are consistent with a broader systematic review and pooled analysis published by Acevedo-Gonzalez and Lacouture-Silgado (2025), which aggregated data from 147 DRG-S salvage patients across multiple centers. The review confirmed that DRG-S salvage has been successfully indicated after failure of every major SCS waveform, including more recent closed-loop and differential-target multiplexed systems, and that clinical outcomes and patient satisfaction are favorable in most appropriately selected cases.
Earlier case series reported similar findings at smaller scale. Yang and Hunter (2017) described two CRPS patients with prior failed traditional SCS who achieved 90% pain reduction with DRG-S salvage, sustained at 8-month follow-up. One patient underwent SCS explantation followed by DRG-S; the other retained the SCS and added DRG-S in a combined system, reporting the strongest relief with DRG-S alone.
For patients whose pain pattern includes both focal and non-focal components, a recent randomized trial (BOOST-DRG, Rigoard et al., 2025) compared SCS alone, DRG-S alone, and combined SCS + DRG-S in patients with persistent spinal pain syndrome after spinal surgery. Each individual modality produced approximately 60% responder rates. The combination approach, when patients could switch between stimulation patterns based on pain characteristics and activity level, raised the responder rate to 80%. Combination therapy is a specific option for specific patients — not a default — but it is a meaningful addition to the salvage toolkit for the right clinical picture.
What This Evidence Is, and What It Isn’t
The salvage evidence base is observational, not randomized. Chapman 2022 is the largest study, but it is retrospective; Acevedo-Gonzalez 2025 pools observational data. What that evidence supports, collectively, is this: DRG-S salvage works meaningfully for appropriately selected failed-SCS patients, and patient selection is the variable that most strongly predicts success. Which is exactly what the next section is about.
The Honest Question: Who Is a Real DRG-S Salvage Candidate?
“SCS failed” is not one clinical category. It is a catch-all phrase that covers several distinct clinical situations, and the situations have different implications for whether DRG-S is the right next step.
Working this out carefully is the whole point of this blog. The response rates in the Chapman 2022 study — NRS 8.7 → 3.8, 93% trial-to-implant conversion, sustained at 34-month follow-up — reflect a specifically selected patient population. They do not reflect what would happen if DRG-S were tried in every patient who has ever failed SCS. To know which group a patient falls into, it helps to name the four common pathways to “failed SCS” directly.
Group 1 — Phenotype Mismatch (The Real DRG-S Salvage Candidates)
These are patients whose pain pattern was never a good fit for dorsal column stimulation in the first place. The clinical picture usually includes focal, dermatomally-distributed neuropathic pain — one foot, one side of the groin, one hand, a specific post-surgical nerve territory. Spinal cord stimulation struggles with this kind of pain because the dorsal columns cover a broad area and cannot easily produce precise, focal stimulation in a specific dermatome. DRG-S was designed for exactly this structural problem.
Patients in Group 1 are the population for whom the Chapman 2022 outcomes apply most directly. This includes most CRPS patients whose SCS did not produce adequate relief, most post-surgical nerve pain patients whose SCS failed to cover the specific territory where the pain lives, and many patients with focal peripheral neuropathy or post-traumatic nerve injury. For these patients, the evidence genuinely supports considering DRG-S as a second-line neuromodulation option — and the trial phase will confirm whether the clinical picture translates into meaningful relief for this specific patient.
Group 2 — Wrong Treatment Modality Altogether
Some patients whose SCS trial failed had pain that was actually structural — pain generated by mechanical nerve compression, spinal instability, or another condition that a surgical or procedural intervention could directly address. For these patients, the SCS trial did not fail due to an incorrect waveform or anatomical target. It failed because neuromodulation was the wrong treatment category for their clinical picture.
This happens more often than the neuromodulation literature fully accounts for. Patients sometimes choose an SCS trial specifically to avoid surgery they are not ready for, and when the trial does not work, the underlying structural problem is still there. For these patients, DRG-S will not help either. What is needed is a reassessment of whether the pain is actually neuromodulation-responsive in the first place, and whether a structural intervention — revision surgery, decompression, stabilization — is the better path.
At Vertrae®, when a patient who has failed SCS presents for evaluation, one of the first questions we ask is whether their clinical picture was ever a true neuromodulation indication, or whether a structural assessment was incomplete before SCS was attempted. For some patients, the honest answer moves the conversation back toward surgical or structural care.
Group 3 — Inadequate or Outdated SCS Trial
Spinal cord stimulation technology has evolved substantially over the past decade. The traditional tonic SCS that was the standard neuromodulation option fifteen years ago is not the same therapy as current-generation burst stimulation (Abbott), closed-loop stimulation (Saluda), or high-frequency 10 kHz SCS (Nevro). The newer waveforms produce different clinical outcomes for specific pain patterns, and a patient whose SCS failure was with older technology may benefit from a different SCS waveform rather than a pivot to DRG-S.
This is particularly relevant for patients with axial low back pain, painful diabetic neuropathy, or diffuse pain patterns, where the newer SCS waveforms have stronger evidence than DRG-S does. For these patients, the right question is not “DRG-S or nothing” — it is “which SCS technology is best suited to this specific clinical picture, and has that actually been tried.” Our companion blog on SCS technology comparison (Blog C in this series) covers this in more detail.
Group 4 — Patient-Level Factors
Some SCS failures were predicted by patient-level factors that the clinical team may or may not have fully addressed at the time of the original evaluation. The most statistically significant of these, specifically for DRG-S outcomes, is chronic opioid use. Hagedorn et al. (2021) demonstrated that chronic opioid use at the time of implantation was associated with significantly lower DRG-S responder rates at 1-month, 3-month, and 12-month follow-up — the only patient characteristic with a statistically significant negative association in their analysis.
Other factors that influence both SCS and DRG-S outcomes include inadequately managed depression, significant pain catastrophizing, untreated substance use concerns, and high-dose ongoing opioid therapy. These are not disqualifying characteristics; many patients with some of these factors do well with neuromodulation after the underlying issue is addressed. But they do mean that the patient’s best next step may not be another neuromodulation trial — it may be addressing the factors that predicted the first failure before attempting a second therapy.
For patients in Group 4, the honest conversation differs from that for Group 1. It is not a question of whether DRG-S targets a different anatomical structure. It is a question of whether the same factors that contributed to the SCS outcome will also shape the DRG-S outcome. That conversation sometimes includes a different sequence of care — working with a pain psychologist, optimizing medication management, or addressing comorbid conditions — before another implant trial is considered.
Clinical Insight — Why “Failed SCS” Is Not One Category
Failed SCS is a catch-all phrase that encompasses four clinically distinct situations: phenotype mismatch (real DRG-S candidates), wrong treatment modality altogether (structural problems requiring different care), inadequate or outdated SCS technology (may benefit from advanced SCS waveforms), and patient-level factors that influence both therapies (may require a different sequence of care first). Each situation has different implications for whether DRG-S is the right next step. Treating them interchangeably is why patients who have failed SCS sometimes cycle through second-line therapies that were never likely to help.
The Role of the Trial in Diagnostic Gray Zones
Most patients will not fit neatly into one of the four groups. Many fit partially into two. Some have a phenotype consistent with Group 1 but also have some Group 4 considerations that influence the odds. For these patients, the clinical picture alone cannot definitively predict whether DRG-S will produce meaningful relief.
This is where the trial phase earns its clinical weight. A 5–7 day DRG-S trial is a reversible, structured way to find out whether the therapy works for this specific patient. It is not a commitment to permanent implantation. It is a diagnostic step, in the most literal sense — information gathering about how this specific nervous system responds to this specific form of stimulation. Patients and physicians often decide, together, that the clinical picture is ambiguous enough that the trial is itself the most useful next step. For appropriately selected patients in the diagnostic gray zones, that decision is not overpromising. It is exactly how neuromodulation is supposed to be used.
What Actually Predicts DRG-S Salvage Success
Moving from the categorical framework to the specific clinical features, the DRG-S salvage literature identifies several factors that meaningfully predict who responds to the therapy.
- Focal, dermatomal pain distribution. The strongest and most consistent predictor across every published study. Patients whose pain lives in a specific nerve territory — one they can point to with a clear boundary — respond to DRG-S more reliably than patients whose pain is widely distributed or multi-regional. The DRG FOCUS multicenter registry (Hunter et al., 2019) found that the extent of the painful area covered by paresthesias during programming was the strongest single predictor of trial success.
- CRPS and peripheral nerve injury as diagnoses. Both populations comprise a substantial share of published salvage outcomes data, and both have been well represented in the literature. CRPS patients are the largest single group in the Chapman 2022 study (n=24 of 60), which is consistent with the broader evidence base showing DRG-S outperforms traditional SCS specifically for CRPS. In the Kretzschmar et al. (2021) three-year follow-up, patients with peripheral nerve injury achieved 73% pain relief at 36 months and 99% opioid reduction in a non-salvage population; the similar phenotype suggests comparable potential in salvage scenarios.
- Distal extremity or groin-region pain. DRG-S is particularly well-suited to anatomical regions that SCS struggles to cover well — foot, ankle, groin, distal nerve distributions. A pooled analysis (Huygen et al., 2020) showed 80% responder rates for groin pain and 75–80% for distal lower-extremity pain, the strongest anatomical regions in the DRG-S literature. Patients whose failed SCS was attributable to poor coverage of these specific regions are particularly plausible salvage candidates.
- Number of leads placed during the trial. Trial protocols using at least two leads per treated area have produced stronger outcomes than single-lead trials. This is a technical factor controlled by the implanting physician, but it matters — and patients evaluating a salvage trial should understand that lead strategy shapes the probability of a successful trial.
- Patent neural foramina. DRG-S lead placement requires the neural foramen to be reasonably patent. Severe foraminal stenosis, extensive epidural scarring from prior spinal surgery, or significantly distorted foraminal anatomy can make standard percutaneous placement technically difficult. Alternative approaches exist — paramedian ipsilateral technique, endoscopic lateral approach, open microsurgical placement — but they require planning and experienced surgical technique. Patients with complex prior surgical history should expect this to be specifically evaluated during the consultation.
Combined SCS + DRG-S therapy, as demonstrated in the BOOST-DRG trial (Rigoard et al., 2025), is an option for patients with a clinical picture that includes both focal and multidermatomal pain components. The combination approach raised responder rates to 80% by allowing patients to switch between stimulation patterns based on pain characteristics and activity level. It is not a default for salvage patients. It is a specific option for specific clinical pictures, and it requires a device system that supports both stimulation modalities.
What Happens at Vertrae® When a Failed-SCS Patient Comes In
Patients who have failed SCS arrive at Vertrae® with a clinical history that is usually more complex than a first neuromodulation evaluation. The evaluation reflects that complexity. It is not a procedural visit or a default path to another trial.
Dr. Kamal Woods reviews the complete clinical picture before making any recommendation. That review includes which SCS technology was trialed or implanted — tonic, burst, high-frequency, or closed-loop; the trial outcome and any loss-of-efficacy pattern over time; the pain pattern as it was and as it has evolved; imaging and relevant diagnostic workup; prior structural interventions and their results; medication history including any chronic opioid therapy; and the patient’s own description of what the pain has done to their daily life.
From that review, the direction of the conversation usually becomes clearer. For patients whose picture fits Group 1 — focal neuropathic pain in a DRG-S-appropriate anatomical distribution, without significant countervailing factors — a DRG-S salvage trial is often the reasonable next step. For patients whose picture suggests Group 2 or Group 3, the conversation often shifts: to structural reassessment, to consideration of advanced SCS waveforms not yet attempted, or to care coordination with pain management or other specialties. For patients with significant Group 4 considerations, the conversation sometimes begins with addressing the factors that predicted the first failure before recommending a second trial.
Every one of those outcomes is a legitimate result of the consultation. The goal is not to route every failed-SCS patient into a DRG-S trial at Vertrae®. The goal is to honestly determine whether DRG-S is likely to help this specific patient — and to say so directly either way.
This blog is not a promise. Most physicians offering DRG-S are trying to help patients who have run out of options; the purpose of writing this carefully is not to critique anyone else doing this work, but to help the patient reading it understand whether DRG-S is likely to be useful for them specifically. What DRG-S offers structurally is a trial phase: 5 to 7 days of temporary stimulation before any permanent hardware is placed. For patients in diagnostic gray zones, the trial itself is often the honest answer to a question the clinical picture alone cannot resolve. If the trial produces meaningful relief, permanent implantation follows. If it does not, the leads come out and the patient has information they did not have before.
At Vertrae® Surgery Center in Dayton, Ohio, Dr. Kamal Woods, MD, MBA, evaluates failed-SCS patients to determine whether DRG-S is appropriate for this specific clinical picture, or whether a different direction — structural reassessment, a different SCS technology, or care coordinated in a different setting — will better serve the patient. Either conversation is a legitimate outcome of the consultation.
Risks and Limitations in the Salvage Setting
Many of the complication considerations for DRG-S salvage are the same as for first-line DRG-S — lead migration (~6%), lead fracture (~6%), infection risk associated primarily with prolonged trial duration, and explantation rates around 12% primarily for insufficient pain relief (Vanloon et al., 2025). Our foundational DRG-S blog provides a more detailed overview of the general risk picture.
Two salvage-specific considerations are worth naming here.
- Existing SCS hardware. Patients with a permanent SCS already in place have several options if DRG-S is pursued: explant the SCS and replace it with DRG-S; retain the SCS and add DRG-S as a separate system with its own pulse generator; or, in specific cases, use a combined system with both SCS and DRG-S leads connected to a single compatible generator. Each approach has technical and clinical trade-offs that are best discussed during the evaluation. Patients should not assume in advance that one approach is universally preferable to another.
- Prior surgical anatomy. Patients whose failed SCS came after prior spinal surgery sometimes have epidural scarring or altered anatomy that makes standard percutaneous DRG-S lead placement more challenging. Alternative approaches exist, including paramedian ipsilateral technique and, in select cases, open microsurgical or endoscopic approaches. These are not barriers to DRG-S, but they do argue for careful planning and for the implanting physician’s specific experience with the therapy — not only with neuromodulation in general.
- The trial outcome itself is an answer. For patients whose salvage trial produces meaningful relief, permanent implantation follows. For patients whose trial does not produce relief, the leads come out, no permanent hardware is placed, and the clinical information gained is itself useful — it confirms that DRG-S is not the tool for this specific clinical picture. That is not a failed evaluation. It is a definitive answer to a previously uncertain question, and it often redirects care toward approaches that are more likely to help.
Hear This Blog as a Podcast
Prefer to listen? This podcast explores why prior SCS failure does not predict DRG-S outcomes, which failed-SCS patients are most likely to benefit from DRG-S salvage, and how the trial phase functions as a reversible diagnostic step — in a format you can listen to on the go.
Read the Full Podcast Transcript
DISCLAIMER: Transcript lightly edited for clarity and readability. The views expressed are intended to explore the full range of clinical considerations in spine care and do not constitute medical advice. For guidance specific to your situation, consult a spine specialist.
TRANSCRIPT TEXT:
Speaker 1: If you’re listening to this right now, I’m guessing you might know exactly what the sterile walls of that clinic room look like.
Speaker 2: Unfortunately, a lot of people do. You might know the exact sympathetic, slightly regretful look your doctor gave you right before they delivered the news — the news that your spinal cord stimulator trial failed. Or maybe you had the permanent implant and it worked for a few months, and then the relief just faded away.
Speaker 1: And then comes the sentence that changes everything. The doctor says: “I’m sorry, but it looks like neuromodulation just isn’t an option for you.” You are gently told that you are completely out of options, and you’re left to figure out how to live the rest of your life with this pain. It’s a devastating conversation, and it happens in clinics every single day.
Speaker 2: Because the underlying assumption in that room is always that the spinal cord stimulator trial was the ultimate, definitive test of your nervous system — like a final exam. You failed. The flawed logic goes: if your body didn’t respond to that one specific electrical therapy, then your body has simply rejected the entire concept of neuromodulation.
Speaker 1: The mission of our deep dive today is to really examine the clinical literature that proves why that “end of the road” framing is usually completely wrong. Today we are drawing from the clinical breakdowns provided by Dr. Kamal Woods on the Vertrae® blog, and we’re going to explore the actual human meaning behind the data.
Speaker 2: We’re going to look at why a failed spinal cord stimulator — or SCS — is not the end of the road. And we’re going to do it by focusing on the mechanisms of the body. No rescue-marketing language, no dramatic promises. Just the science.
Speaker 1: Because the reason that “end of the road” framing is fundamentally flawed isn’t based on some new abstract theory. It’s purely anatomical. The clinical literature shows that spinal cord stimulation and an entirely different therapy called dorsal root ganglion stimulation, or DRG-S, target completely different physical structures. The failure of one simply doesn’t dictate the failure of the other, because they aren’t doing the same job.
Speaker 2: Before we get into the statistics or the clinical trials, I want to ground this. If I’m a patient who’s been sitting at home for six months, completely demoralized because I was told my nervous system doesn’t respond to electricity, I’m going to be skeptical. So why should I believe this? Can we break down the actual anatomy? What are we talking about when we say SCS versus DRG-S?
Speaker 1: Think about the anatomy of your spine and your nervous system as a massive transit network. Traditional spinal cord stimulation targets a structure called the dorsal columns of the spinal cord. To do this, the electrodes are placed in the epidural space — the area just outside the protective sac of the spinal cord, over the midline of the back. When you stimulate those dorsal columns, you produce broad, diffuse effects. You’re essentially casting a wide net over a large anatomical region.
Speaker 2: So when you say dorsal columns in the midline, we are basically talking about the main interstate highway of the nervous system.
Speaker 1: Exactly. And casting that wide net is effective if a patient has diffuse, multi-regional pain — say, pain that radiates across the lower back and down both legs. But it is imprecise. If the pain is focal — if it lives in one distinct area — that broad net often passes right over it.
Speaker 2: It’s like being told electricity doesn’t work in your entire house because the hallway floodlights burned out, when all you really needed was to fix the wiring to one specific reading lamp in the corner. So what is DRG-S doing differently?
Speaker 1: DRG-S targets the dorsal root ganglion. To picture this, don’t look at the main highway of the spinal cord — look at the neural foramen. These are the small bony openings on the sides of your vertebrae where individual nerve roots exit the spine. The dorsal root ganglion is a dense cluster of sensory nerve cell bodies sitting in that opening. It acts as the exact gateway where pain signals from a single dermatome — one specific nerve territory, like your left foot or your right knee — enter the spine.
Speaker 2: So it’s literally acting as a checkpoint.
Speaker 1: Precisely. It is a checkpoint. By targeting the DRG, you are acting on those specific sensory cell bodies before the pain signals ever reach the main highway of the spinal cord.
Speaker 2: So the spinal cord is like a massive, chaotic nightclub. Traditional SCS is like trying to quiet the entire room by yelling over the music. DRG-S is like placing a bouncer right at the specific side door where the troublemakers are trying to get in, and turning them away before they ever hit the dance floor.
Speaker 1: That’s exactly how it works. The DRG is the bouncer. It’s the checkpoint. And because you are targeting that checkpoint instead of the whole room, you can use a fraction of the energy — and you don’t get the widespread tingling sensations that traditional SCS usually causes.
Speaker 2: I have to push back here for a second. If the anatomy is so distinctly different — if the main highway is so clearly different from the side door checkpoint — why did my doctor tell me my neuromodulation options were exhausted? Why is there so much false finality in that clinic room?
Speaker 1: It really comes down to medical history and clinical habit. For decades, spinal cord stimulation was essentially the only major neuromodulation tool available. It was the only hammer in the toolbox. Because it was the only tool, the medical community treated it as a catch-all. It was applied to almost all chronic nerve pain. It wasn’t viewed as a highly specific tool for one highly specific anatomical target. It was the default. We’re now in an era of precision medicine, but those old habits die hard. The literature now clearly shows us that because they target completely different structures, the failure of an SCS trial has no predictive value for DRG-S outcomes.
Speaker 2: Not at all?
Speaker 1: Not at all. Failing a trial on the main highway simply means the first tool was aimed at the wrong target for your specific type of pain.
Speaker 2: Let’s be realistic, though. If we are going to talk about a second chance at pain relief, we have to talk about who this is not for. One of the things I really appreciated about the Vertrae® blog breakdown is that it actively filters people out. It introduces the concept that saying “SCS failed” is actually a completely useless catch-all phrase.
Speaker 1: It is a linguistic shortcut that doctors use, but it masks four entirely distinct clinical realities. And if we want to be medically responsible here, we really need to unpack those four groups.
Speaker 2: Let’s walk through them. Because this might help someone listening figure out exactly why their first trial didn’t work.
Speaker 1: Group one is what the clinical literature calls phenotype mismatch. This is the patient whose original pain was highly focal — in one specific dermatome. A single foot after a crush injury, a specific knee after a botched surgery, or a classic case of complex regional pain syndrome, or CRPS.
Speaker 2: CRPS is when the nervous system essentially gets stuck in a severe localized feedback loop of pain, swelling, and temperature changes. The pain is intensely severe but highly localized.
Speaker 1: For a group-one patient, the traditional spinal cord stimulator was simply the wrong tool for the job. The net was too wide to capture the localized pain. These are the true DRG-S candidates. Their pain is exactly what dorsal root ganglion stimulation was engineered to treat.
Speaker 2: Then we have group two. This is the group where the failure was due to the wrong treatment modality altogether — meaning the pain wasn’t a nerve-signaling issue that an electrical device could fix in the first place.
Speaker 1: Exactly. This often involves a structural issue. A patient might have a mechanically compressed nerve — physical structural pinching in the lumbar spine from a herniated disc or severe stenosis. Patients — and honestly, sometimes their doctors — will try an SCS trial because they desperately want to avoid a major spinal fusion or decompression surgery.
Speaker 2: Which is entirely understandable. Spine surgery is daunting. But if you have a structurally crushed nerve, laying an electrical wire over it isn’t going to uncrush the nerve.
Speaker 1: Electricity cannot remove a bone spur. If your trial failed because you actually needed structural surgery, then putting a DRG-S device in isn’t going to help either. You need the structural issue addressed.
Speaker 2: Group three: inadequate or outdated trial. This one is fascinating to me because it’s about the technology itself.
Speaker 1: This is the patient who failed an old traditional SCS trial years ago and gave up. Technology in neuromodulation moves quickly. A patient in group three might actually have the kind of diffuse, multi-regional back and leg pain that is well-suited to spinal cord stimulation, but they failed a device from eight or ten years ago. Those older devices used tonic stimulation, which relies on replacing pain with a constant tingling sensation called paresthesia. Many patients couldn’t tolerate the tingling. It was too distracting.
Speaker 2: So they don’t need DRG-S — they need an updated version of SCS.
Speaker 1: Correct. They might need a modern SCS system using burst stimulation or 10 kHz therapy, which operates at such a high frequency that the patient doesn’t feel any tingling at all. The therapy simply smooths out the pain signals in the background. They just need the modern version of the tool they already tried.
Speaker 2: And finally, group four: patient-level factors. This is a delicate one, but it’s crucial.
Speaker 1: This refers to a trial that was derailed by outside factors — unmanaged severe depression, or high-dose chronic opioid use. It requires a very honest conversation between the care team and the patient, because if those systemic factors aren’t addressed, they will likely sabotage a DRG-S trial just as they sabotaged the first one.
Speaker 2: This brings us to a tough piece of clinical data. If we’re talking about blind spots and who this therapy fails for, we have to look at the Hagedorn 2021 study, because researchers specifically analyzed patient characteristics to see what actually predicted failure with DRG-S.
Speaker 1: They did. And out of all the variables they examined, they found exactly one patient characteristic that had a statistically significant negative association with DRG-S outcomes. That characteristic was chronic opioid use at the time of implantation.
Speaker 2: I want to make sure we explain the how and why behind this, because I can hear a patient listening right now getting frustrated. If someone has been in agony for years with CRPS or a nerve injury, of course they’re on opioids. They’re just trying to survive the day. Why does taking a pain medication stop an electrical device from working? It sounds almost contradictory.
Speaker 1: It’s a great question, and it’s crucial to understand that this is not a moral judgment by the medical community. It is strictly physiological. High-dose chronic opioid therapy changes the neuroplasticity of your central nervous system — it literally changes the physical wiring. Over time, as your body builds a tolerance to the opioids, it attempts to maintain equilibrium by creating more pain receptors. It’s a condition called opioid-induced hyperalgesia. Your nervous system becomes hypersensitized. It’s on high alert, constantly looking for pain signals. So when you introduce the subtle, targeted electrical pulses of a DRG stimulator, the system is too ramped up by the medication’s aftereffects to perceive the relief. The electricity is trying to quiet down a system that the medication is inadvertently keeping on high alert.
Speaker 2: What does that mean practically for the patient? Are they permanently disqualified from trying DRG-S?
Speaker 1: Absolutely not. It doesn’t mean they are disqualified, but it dictates the sequence of their care. If you rush straight into a DRG-S trial without addressing the medication load first, you are drastically lowering your own odds of success. The responsible medical approach is to work with your pain management team to safely optimize — and if appropriate, taper or reduce — the opioid load, allow the nervous system to resensitize and calm down, and then approach the trial. You want to prepare the environment so the device has a chance to work.
Speaker 2: You’re preparing the soil before you plant the seed. So let’s look at the best-case scenario. Say we have a patient who falls cleanly into group one. They have focal, localized pain. Their medications are optimized. They are the textbook candidate for DRG-S. What actually happens when they try it? This is where the Chapman 2022 salvage study comes in, and the numbers here are, frankly, hard to wrap my head around.
Speaker 1: The Chapman 2022 dataset is important because it is the largest published study looking specifically at DRG-S as a salvage therapy — meaning using it to rescue patients who had already failed a spinal cord stimulator. They tracked 60 patients, and every single one of them had a documented failure with traditional SCS.
Speaker 2: So 60 patients who were already told it was over.
Speaker 1: And these were specifically group-one patients. They had focal neuropathic pain, primarily CRPS or localized post-surgical nerve pain. So they were carefully selected. Out of those 60 patients who had already failed neuromodulation, 56 of them had a successful temporary DRG-S trial and moved on to receive the permanent implant. That is a 93% trial-to-implant conversion rate.
Speaker 2: I want to pause and let that land. That number is striking, because we’re talking about a cohort of people sitting in that exact clinic room we described at the beginning. They were specifically told their bodies did not respond to this technology — and 93% of them responded to it.
Speaker 1: It really highlights how important anatomical targeting is. And we have to look at the pain scores too. The study measured their baseline pain before the DRG-S trial, and the average was an 8.7 out of 10.
Speaker 2: If we translate that from a clinical chart into real human life, living at an 8.7 every single day is not really living. It’s a state of exhausting survival. Your world shrinks. You aren’t going to the park. You aren’t sleeping through the night. You are bracing against a sensory assault all day long.
Speaker 1: After the DRG-S therapy, that average pain score dropped from 8.7 to 3.8.
Speaker 2: Dropping to a 3.8 is the difference between being bed-bound and being able to go to the grocery store. It’s being able to sit through a movie. It’s getting a version of your life back.
Speaker 1: And just as importantly, the relief was shown to be durable. The study demonstrated that relief was sustained at a median follow-up of nearly three years, with an explant rate of only 3.6%.
Speaker 2: Can you define explant rate for us?
Speaker 1: Explant rate refers to the percentage of patients who had to have the permanent device surgically removed, either because it stopped providing relief over time or due to complications like an infection. A 3.6% explant rate over three years is remarkably low. It shows that this isn’t a temporary placebo effect. The therapy isn’t wearing off quickly. When you hit the correct anatomical checkpoint — the DRG bouncer we talked about — the therapy holds.
Speaker 2: The data is compelling. But I want to play devil’s advocate. Put yourself in the shoes of a patient who has already gone through the physical — and honestly, the psychological — trauma of a failed medical procedure. You got your hopes up. You went through a trial or an implant surgery, and it failed. The idea of volunteering your body for another invasive procedure — the skepticism and the fear are immense. How does a doctor actually ask a patient to take that leap of faith again?
Speaker 1: Medical trauma is very real, and the hesitation is justified. But this is where the actual mechanism of how neuromodulation is delivered becomes important. You aren’t signing up for a massive, irreversible surgery based on a doctor’s hunch. DRG-S, like traditional SCS, begins with a temporary trial phase.
Speaker 2: Walk me through what that actually feels like for the patient. What does a “temporary trial” mean practically?
Speaker 1: It’s a five-to-seven-day test drive. Thin, flexible temporary leads — essentially tiny wires — are placed percutaneously.
Speaker 2: Percutaneously — meaning through the skin, like an epidural injection rather than a large surgical incision?
Speaker 1: Exactly. They are introduced through a needle in the lower back, guided to the DRG checkpoint, and taped securely to your skin. Those wires are connected to a small external battery pack that you wear on a belt around your waist. And then you leave the clinic. You go home. There is no permanent hardware placed inside your body. You spend a week sleeping in your own bed, walking around your own kitchen, and you see firsthand whether it changes your pain.
Speaker 2: I really appreciate the structural and diagnostic honesty of that process. It isn’t a doctor saying, “Let’s permanently fuse your spine and cross our fingers.” It’s the doctor saying, “Let’s ask your nervous system a very specific question, and let’s see how it answers in real time.”
Speaker 1: It is a fully reversible diagnostic test. If you spend that week and your pain drops from an 8 to a 3 and you get your mobility back, then — and only then — do you schedule the procedure to have the tiny permanent battery implanted under the skin.
Speaker 2: But what if it doesn’t work? What if you go through the week and the pain is exactly the same?
Speaker 1: You go back to the clinic, the doctor gently pulls the temporary wires out — which is done in the office — and you put a bandage on it and go home. You haven’t burned any bridges anatomically.
Speaker 2: And honestly, I would argue that even if the trial “fails,” it is still a meaningful clinical success for the patient.
Speaker 1: How do you mean?
Speaker 2: Because the patient walks away with definitive diagnostic information about their own body that they did not have a week ago. If you do the DRG-S trial and your pain doesn’t change, you now know for a fact that your pain is not being driven entirely by that specific dorsal root ganglion. You have definitively crossed a major suspect off the list. That narrows the field, and it forces your care team to look somewhere else to figure out what is actually wrong.
Speaker 1: That is an astute clinical perspective. In medicine, ruling something out is often as valuable as ruling something in. The trial outcome itself provides clarity. It resolves a diagnostic gray area without requiring a permanent commitment.
Speaker 2: As we pull all these threads together, I want to be specific about who this deep dive is for today. This information is targeted at patients who have already had a failed spinal cord stimulator — meaning either the initial trial didn’t provide relief, or the permanent implant eventually stopped working. But crucially, it is for patients in that group whose pain is highly focal.
Speaker 1: Group one. It is dermatomally distributed neuropathic pain, meaning you can point to exactly where it hurts — a foot, a groin, a knee — and the pain stays localized in that specific territory. Specifically, patients dealing with complex regional pain syndrome, or CRPS, or pain from a distinct peripheral nerve injury. If that sounds like your clinical picture, the data from Chapman and the anatomical science suggest that your neuromodulation journey may not actually be over.
Speaker 2: And if you fall into that category, the logical next step is a rigorous, honest evaluation. The evaluation process at Vertrae® with Dr. Kamal Woods is structured to do exactly what we’ve spent this time discussing today — to carefully filter through those four groups and determine whether DRG-S actually fits your specific anatomy.
Speaker 1: And remember, the purpose of seeking out that consultation is not to push you into signing up for another trial. The purpose is diagnostic. It is to figure out if you belong in group one, or if a completely different direction — like addressing a structural issue or updating to a newer SCS technology — makes more clinical sense for you. Either answer gives you a roadmap.
Speaker 2: If you want to learn more about that process or request a consultation, you can find that information at vertrae.com.
Speaker 1: The ultimate goal is to find the truth of what is happening in your anatomy.
Speaker 2: I want to leave you with a final thought — something that shifted my own perspective as we were analyzing this clinical data. We are deeply conditioned to view a failed medical trial as a personal dead end. When a device doesn’t work, it is easy to internalize that failure — to feel like it’s a failing of your own body, to feel like your nervous system is somehow broken beyond repair. But what if we stopped looking at it that way? What if we started viewing a failed trial simply as a necessary, neutral data point? A failed spinal cord stimulator on the main highway of your spine did not mean your body was broken. It was your nervous system’s way of telling your doctor where not to look. The main highway was the wrong place to check. And by crossing it off the list, that failure actually moved you one step closer to finding the specific anatomical checkpoint — the right side door — that may hold the answer.
Speaker 1: You aren’t at the end of the road. You might just finally have the exact map you need to find the right one.
Key Takeaway
For patients whose spinal cord stimulator did not produce the relief everyone hoped for, or whose SCS worked for a time and has gradually stopped — the clinical reality is more specific than “neuromodulation failed.” SCS and DRG-S target different structures through different mechanisms, and prior SCS failure does not predict what DRG-S will do for any individual patient. For patients whose pain pattern is focal and dermatomal, particularly CRPS or peripheral nerve injury, the salvage evidence is genuinely encouraging. For patients whose pain pattern was never a neuromodulation problem in the first place, or whose original SCS failure reflected factors DRG-S cannot address, a different direction is the honest answer. At Vertrae® Surgery Center in Dayton, Ohio, Dr. Kamal Woods evaluates failed-SCS patients to determine, honestly, which direction is most likely to help.
Frequently Asked Questions
My SCS trial failed. Does that mean neuromodulation isn’t going to work for me?
Not necessarily — it depends on why the SCS trial failed. SCS and DRG-S target different anatomical structures, and prior SCS failure has no predictive value for DRG-S outcomes in patients whose pain pattern matches DRG-S indications (Chapman et al., 2022). The more useful question is whether your specific pain pattern was ever a good fit for spinal cord stimulation in the first place, or whether it would have been a better fit for a different neuromodulation approach, a different SCS waveform, or possibly a different category of treatment altogether. The evaluation at Vertrae® is designed to work out exactly that question.
My SCS worked for a year or two and now it doesn’t. Is DRG-S really different?
The loss-of-efficacy pattern has been well-documented with traditional SCS — an effect called therapy habituation, where pain relief gradually diminishes over months of follow-up (Levy et al., 2020). The same substudy of the ACCURATE trial that documented this habituation pattern with SCS did not find it with DRG-S, where pain relief remained stable across 12-month follow-up without significant attenuation. That mechanistic difference is part of why DRG-S is specifically considered for patients whose SCS has lost efficacy. Whether it will produce relief for your specific clinical picture is what the evaluation and, if appropriate, the trial will determine.
Do I have to have my current SCS removed to try DRG-S?
Not necessarily. Several technical options exist, depending on your specific situation. Some patients explant the SCS and replace it with DRG-S. Others retain the SCS system and add DRG-S as a separate system, preserving the option to use either modality depending on pain characteristics. In specific cases, a combined system connecting both SCS and DRG-S leads to a single compatible pulse generator is appropriate. The right approach depends on your clinical picture and is determined during the consultation.
How is trying DRG-S different from just trying a newer SCS waveform like burst or closed-loop?
This is a genuinely important question. Advanced SCS waveforms — burst stimulation, closed-loop stimulation, high-frequency 10 kHz — have produced better outcomes than traditional tonic SCS for certain pain patterns, and for some failed-SCS patients the right next step is actually a different SCS waveform rather than DRG-S. Which direction makes sense depends on your pain pattern. If the pain is focal and dermatomal (particularly CRPS, peripheral nerve injury, or focal post-surgical pain), DRG-S is likely the more appropriate next step. If the pain is more diffuse, axial, or multi-dermatomal, an advanced SCS waveform may be the stronger choice. Our companion blog on SCS technology comparison covers the specific waveforms in detail, and the evaluation at Vertrae® considers both directions.
If the DRG-S trial also doesn’t work, what then?
An unsuccessful DRG-S trial is not a dead end. It is clinical information that was not available before. For some patients, it confirms that the pain is not neuromodulation-responsive as the initial evaluation suggested, and the next step is usually a reassessment of the underlying pain mechanism — sometimes including structural reassessment, sometimes including broader pain-management coordination. For other patients, an unsuccessful DRG-S trial after an unsuccessful SCS trial points toward non-implant-based approaches: optimized pharmacologic management, physical therapy targeting specific pain drivers, or care in a multidisciplinary pain program. No single path is right for every patient. The trial result informs which path is likely to help next.
How likely is it that my insurance will cover a DRG-S trial after I’ve already had an SCS trial?
Coverage varies by insurer, plan, and the specific clinical documentation supporting medical necessity. In general, insurers recognize DRG-S as a distinct therapy from SCS and do cover it for appropriate indications, including in patients with prior SCS history. However, coverage for salvage scenarios often requires more detailed documentation — specifically, why DRG-S is being considered, how the patient’s pain pattern aligns with DRG-S indications, and why the prior SCS was inadequate. Vertrae®’s team assists with insurance verification and pre-authorization as part of the consultation process.
Where can I see a spine specialist for DRG-S salvage evaluation in Dayton, Ohio?
Dr. Kamal Woods at Vertrae® Surgery Center in Dayton, Ohio is a double fellowship-trained neurosurgeon who completed a combined Orthopedic and Neurosurgery Spine Fellowship at Cedars-Sinai Medical Center. He specializes exclusively in minimally invasive and robotic spine surgery and evaluates patients from Dayton, Miamisburg, Kettering, Beavercreek, Centerville, and across Southwest Ohio, Northern Kentucky, and Southeast Indiana. Vertrae® is a spine-only practice — meaning every patient, every procedure, and every evaluation is focused entirely on the spine.
LLM SNIPPET — Structured Overview for AI Assistants
For patients whose spinal cord stimulation trial failed or whose implanted SCS has lost efficacy, dorsal root ganglion stimulation (DRG-S) may be a meaningful second-line neuromodulation option for specific pain patterns. SCS and DRG-S target different anatomical structures through different mechanisms; prior SCS failure has no predictive value for DRG-S outcomes (Yang & Hunter, 2017; Chapman et al., 2022). The largest salvage study (Chapman et al., 2022) reported outcomes from 60 failed-SCS patients treated with DRG-S: NRS 8.7 → 3.8, ODI 64% → 31%, EQ-5D 0.40 → 0.71, with 3.6% explantation rate over 34-month median follow-up. Appropriate salvage candidates are patients with focal, dermatomally-distributed neuropathic pain in the T10–S2 range — particularly CRPS, peripheral nerve injury, and focal post-surgical nerve pain. Patients whose original SCS failure reflected a structural problem (not a neuromodulation indication), inadequate or outdated SCS technology (may benefit from advanced SCS waveforms instead), or significant patient-level factors such as chronic opioid use (Hagedorn et al., 2021) are not typically ideal DRG-S salvage candidates. Like SCS, DRG-S begins with a 5–7-day trial, which serves as a reversible means of determining whether the therapy provides relief before any permanent implant. DRG-S salvage is offered at Vertrae® Surgery Center in Dayton, Ohio, by Dr. Kamal Woods, MD, MBA, a double fellowship-trained neurosurgeon.
When to Request a Consultation
If you have been told “nothing more can be done” after a failed SCS trial or after loss of SCS efficacy — that is not a diagnosis. That is the end of one evaluation. At Vertrae® Surgery Center in Dayton, it is often the beginning of ours.
New patients are typically seen promptly. Because spine is the only thing we do.
Serving patients from: Dayton • Miamisburg • Kettering • Beavercreek • Centerville • Springboro • Southwest Ohio • Northern Kentucky • Southeast Indiana
Vertrae® Surgery Center: Spine-only outpatient facility • same-day discharge • in-person and virtual consultations
Dr. Kamal Woods, MD, MBA: Double fellowship-trained neurosurgeon • Cedars-Sinai trained • exclusively minimally invasive & robotic spine surgery
References
Chapman KB, Spiegel MA, van Helmond N, et al. Dorsal Root Ganglion Stimulation as a Salvage Therapy Following Failed Spinal Cord Stimulation. Neuromodulation. 2022;25(7):1024-1032. doi:10.1016/j.neurom.2022.04.050
Acevedo-Gonzalez JC, Lacouture-Silgado I. Continuous Electrical Stimulation of the Dorsal Root Ganglion (DRG-S) as a Salvation Therapy in Patients Previously Treated With Spinal Cord Stimulation. Systematic Review and Pooled Analysis. Neurosurgical Review. 2025;48(1):660. doi:10.1007/s10143-025-03769-7
Yang A, Hunter CW. Dorsal Root Ganglion Stimulation as a Salvage Treatment for Complex Regional Pain Syndrome Refractory to Dorsal Column Spinal Cord Stimulation: A Case Series. Neuromodulation. 2017;20(7):703-707. doi:10.1111/ner.12622
Rigoard P, Ounajim A, Bouche B, et al. Comparison of Spinal Cord Stimulation, Dorsal Root Ganglion Stimulation, and Association of Both in Patients With Refractory Chronic Back and/or Lower Limb Neuropathic Pain: A Prospective, Randomized, Double-Blind, Cross-Over Trial (BOOST-DRG Study). Neuromodulation. 2025;28(2):283-296. doi:10.1016/j.neurom.2024.10.003
Levy RM, Mekhail N, Kramer J, et al. Therapy Habituation at 12 Months: Spinal Cord Stimulation Versus Dorsal Root Ganglion Stimulation for Complex Regional Pain Syndrome Type I and II. The Journal of Pain. 2020;21(3-4):399-408. doi:10.1016/j.jpain.2019.08.005
Hagedorn JM, McArdle I, D’Souza RS, et al. Effect of Patient Characteristics on Clinical Outcomes More Than 12 Months Following Dorsal Root Ganglion Stimulation Implantation: A Retrospective Review. Neuromodulation. 2021;24(4):695-699. doi:10.1111/ner.13326
Hunter CW, Sayed D, Lubenow T, et al. DRG FOCUS: A Multicenter Study Evaluating Dorsal Root Ganglion Stimulation and Predictors for Trial Success. Neuromodulation. 2019;22(1):61-79. doi:10.1111/ner.12796
Huygen FJPM, Kallewaard JW, Nijhuis H, et al. Effectiveness and Safety of Dorsal Root Ganglion Stimulation for the Treatment of Chronic Pain: A Pooled Analysis. Neuromodulation. 2020;23(2):213-221. doi:10.1111/ner.13074
Kretzschmar M, Reining M, Schwarz MA. Three-Year Outcomes After Dorsal Root Ganglion Stimulation in the Treatment of Neuropathic Pain After Peripheral Nerve Injury of Upper and Lower Extremities. Neuromodulation. 2021;24(4):700-707. doi:10.1111/ner.13222
Deer TR, Levy RM, Kramer J, et al. Dorsal Root Ganglion Stimulation Yielded Higher Treatment Success Rate for Complex Regional Pain Syndrome and Causalgia at 3 and 12 Months: A Randomized Comparative Trial. Pain. 2017;158(4):669-681. doi:10.1097/j.pain.0000000000000814
Vanloon M, Van Broeckhoven T, Raymaekers V, et al. Noninfectious Complications of Dorsal Root Ganglion Stimulation: A Systematic Review and Meta-Analysis. Neuromodulation. 2025;28(2):234-248. doi:10.1016/j.neurom.2024.10.010
Chapman KB, Sayed D, Lamer T, et al. Best Practices for Dorsal Root Ganglion Stimulation for Chronic Pain: Guidelines From the American Society of Pain and Neuroscience. Journal of Pain Research. 2023;16:839-879. doi:10.2147/JPR.S364370
